Sudden Intense Chest Pain Unlike Prior Pneumothorax

Medscape

07-07-2025

Editor's Note:
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Background and Initial Presentation
A 35-year-old man with a history of two prior spontaneous pneumothoraxes — both managed conservatively — presents to the emergency department with new-onset chest pain and lightheadedness. The pain is described as sudden, intense, and exacerbated by deep breathing. He indicates that it is located in the center of the chest. He denies dyspnea or leg swelling and has no other complaints. When asked, he says this pain is different from his pneumothorax pain, mainly because it is in the center of his chest.
Physical Examination and Workup
Vital signs are within normal limits, except for a pulse > 120 bpm. Physical examination reveals diminished breath sounds on the left hemithorax. There are no rales or wheezes and no leg edema.
Discussion
Central pleuritic chest pain in a patient with a history of pneumothorax suggests a pulmonary etiology. A chest x-ray is the most appropriate investigation to promptly assess for recurrent pneumothorax, pleural effusion, structural abnormalities, or other intrathoracic pathology.
ECG or cardiac biomarkers such as troponins are indicated primarily if myocardial ischemia or infarction is suspected. This suspicion would be raised if the patient described his chest pain as squeezing or pressure-like sensation radiating to the neck, jaw, or left arm. The patient's young age and lack of history of coronary artery disease also make acute coronary syndrome less likely.
A CBC may provide supplementary information about signs of infection or inflammation, especially if the chest x-ray appears normal, but a CBC alone is unlikely to determine the cause of the patient's acute pleuritic chest pain.
On initial testing, chest x-ray, metabolic panel, and troponin level were normal. CBC showed an elevated white blood cell count (16,200/μL). An ECG was also performed (Figure 1).
Figure 1. ECG performed on patient in ED.
Despite the central location of symptoms, the patient's young age, history of pneumothorax, and presence of pleuritic chest pain would have placed pneumothorax high on the initial differential diagnosis. After pneumothorax was ruled out with chest x-ray, PE should have become the leading consideration given the pleuritic pain and the patient's age group, in which PE is far more common than coronary artery disease. Although anxiety is also common in this age group — as it is in others — it should remain a diagnosis of exclusion, considered only after more serious conditions have been reasonably ruled out.
While the ECG is not diagnostic of PE, it raises suspicion by demonstrating three supportive findings: tachycardia, incomplete right bundle branch block, and nonspecific ST-segment changes.[1] A subsequent D-dimer test was positive, and chest CT angiography showed extensive bilateral pulmonary emboli, more pronounced on the left side.
PE typically presents as either unilateral pleuritic chest pain or as dyspnea with or without chest pain.[1] However, PE can present without the typical symptom of chest pain, sometimes being asymptomatic or discovered incidentally during diagnostic workup for other conditions.[1,2,3] Other symptoms of large pulmonary emboli may include syncope, diaphoresis, and cardiac arrest. Other symptoms of smaller emboli may include minor hemoptysis or cough.[1,3]
Although most patients with PE have at least one identifiable risk factor, up to 20% of patients present without any known risk factor, so the absence of risk factors should not exclude the diagnosis.[1]
Pain in patients with PE is believed to result from pulmonary infarction, which typically occurs when small to medium emboli lodge distally in the peripheral pulmonary arteries — areas with limited collateral circulation — making them more susceptible to infarction. The absence of chest pain does not exclude PE and may contribute to missed diagnoses, increasing the risk of patient morbidity and mortality.
PE classically presents with pleuritic chest pain and dyspnea associated with known risk factors, tachycardia, and clear lungs both on auscultation and chest radiography. However, most patients with PE present with one or more atypical features, which may include the absence of pain or any known risk factors and/or normal or nonspecific ECG findings.[1] About 40% of patients with PE have tachycardia.[1]
Scoring systems such as the PE Rule-out Criteria (PERC) can be useful in evaluating patients with suspected PE, but clinicians must be familiar with both the inclusion and exclusion criteria and should recognize that applying PERC requires a low pretest probability based on clinical judgment and the presence of a more likely alternate diagnosis with adequate supporting evidence.
When PE cannot be excluded based on clinical assessment, diagnostic testing is warranted, typically beginning with a D-dimer assay. If the D-dimer is positive, imaging with CT pulmonary angiography or a or ventilation-perfusion scan should follow.[2,3] D-dimer should not be ordered reflexively or 'just in case,' as this often leads to unnecessary imaging. As Greg Henry advises, 'In medicine and life, don't ask questions you don't really want to know the answer to.'
PE is typically treated with anticoagulants unless they are absolutely contraindicated, in which case a vena cava interruption filter may be used.[2,3,4] The treatment setting and choice of anticoagulant depend on various factors, including PE severity, comorbidities, and bleeding risk.[3] Most patients are admitted for treatment initiation, but some low-risk patients may be discharged with oral anticoagulants.[2] Patients with hypotension or right ventricular strain often require ICU admission for close monitoring and may be treated with thrombolytic therapy or, in some cases, surgical intervention.[1,2,3]
The absolute contraindication to thrombolytic therapy is a history of intracranial hemorrhage, due to a significantly increased risk of catastrophic bleeding.[1,2,4] Thrombolytic agents can dissolve blood clots, but they also impair hemostasis.
A history of pneumothorax episodes is not considered an absolute contraindication to thrombolytics in this patient.[1] Anemia is an important clinical factor that significantly increases the risk of bleeding during anticoagulation, but it does not preclude thrombolysis, if not caused by active bleeding or associated with a significant coagulopathy.[1,3,5]
Hemodynamic instability is not a contraindication but rather an indication for thrombolytic therapy in patients with massive PE. The benefits of restoring circulation outweigh the bleeding risk associated with thrombolysis.[1,2,4]
Hospital admission on intravenous heparin is reasonable. The patient could deteriorate if additional thrombi embolize. ICU admission is typically reserved for patients who remain unstable or require intravenous fibrinolytics. Discharge may be appropriate for stable patients who meet discharge criteria. For patients who are stable but do not qualify for discharge and have a low risk of decompensation, admission to a general medical floor may be considered.
Because this patient's CT angiography showed extensive PE and his vital signs were concerning, thrombolytics were considered. However, after heparin was initiated, his vital signs normalized within a few hours, so he was able to be admitted to a telemetry bed.
Although most patients with PE meet criteria for outpatient treatment,[3,4] a minority of eligible patients are actually discharged from the emergency department despite having an estimated mortality risk of less than 3%.[1,2] Risk stratification tools such as the Pulmonary Embolism Severity Index and the Hestia criteria can help identify candidates for outpatient treatment. Clinicians should also consider using an online calculator (eg, MDcalc.com). In addition to PE severity, clinicians should evaluate the patient's bleeding risk on anticoagulation when making disposition decisions.[1,2,3,4]